title: Marked elevation of brain natriuretic peptide levels in pericardial fluid is closely associated with left ventricular dysfunction.
abstract: OBJECTIVE
  The purpose of this study was to investigate whether atrial and brain natriuretic peptides (ANP and BNP, respectively) represent autocrine/paracrine factors and are accumulated in pericardial fluid.
  
  
  BACKGROUND
  ANP and BNP, systemic hormones produced by the heart, have elevated circulating levels in patients with heart failure. Recent evidence suggests that the heart itself is one of the target organs for these peptides.
  
  
  METHODS
  With an immunoreactive radiometric assay, we measured the concentrations of these peptides in plasma and pericardial fluid simultaneously in 28 patients during coronary artery bypass graft surgery.
  
  
  RESULTS
  The pericardial levels of BNP were markedly elevated in patients with impaired left ventricular function. We investigated the correlation of ANP and BNP levels in plasma or pericardial fluid with left ventricular hemodynamic variables. None of the hemodynamic variables correlated with ANP levels in plasma or pericardial fluid. Both plasma and pericardial fluid levels of BNP were significantly related to left ventricular end-diastolic and systolic volume indexes (LVEDVI and LVESVI, respectively). In addition, BNP pericardial fluid levels had closer relations with LVEDVI (r = 0.679, p < 0.0001) and LVESVI (r = 0.686, p < 0.0001) than did BNP plasma levels (LVEDVI: r = 0.567, p = 0.0017; LVESVI: r = 0.607, p = 0.0010). BNP levels in pericardial fluid but not in plasma correlated with left ventricular end-diastolic pressure (r = 0.495, p = 0.0074).
  
  
  CONCLUSIONS
  BNP levels in pericardial fluid served as more sensitive and accurate indicators of left ventricular dysfunction than did BNP levels in plasma. Thus, BNP may be secreted from the heart into the pericardial space in response to left ventricular dysfunction, and it may have a pathophysiologic role in heart failure as an autocrine/paracrine factor.
authors.affiliation: Takeda Hospital, Kyoto, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Hasegawa
authors.forename: M
authors.initials: M
authors.lastname: Fujita
authors.forename: S I
authors.initials: SI
authors.lastname: Tamaki
authors.forename: A
authors.initials: A
authors.lastname: Yamazato
authors.forename: Y
authors.initials: Y
authors.lastname: Kihara
authors.forename: R
authors.initials: R
authors.lastname: Nohara
authors.forename: S
authors.initials: S
authors.lastname: Sasayama
mesh_terms: D000368:Aged; D009320:Atrial Natriuretic Factor / Q000032:analysis / Q000097:blood; D019898:Autocrine Communication; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D002303:Cardiac Output, Low / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D002306:Cardiac Volume / Q000502:physiology; D001026:Coronary Artery Bypass; D003327:Coronary Disease / Q000601:surgery; D003971:Diastole; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008944:Mitral Valve Insufficiency / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D020097:Natriuretic Peptide, Brain; D009419:Nerve Tissue Proteins / Q000032:analysis* / Q000097:blood; D019899:Paracrine Communication; D010490:Pericardial Effusion / Q000737:chemistry*; D011863:Radioimmunoassay; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000378:metabolism*; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D015415:Biomarkers; D009419:Nerve Tissue Proteins; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor